Aggravation of Seizures and/or EEG Features in Children Treated with Oxcarbazepine Monotherapy

Vendrame, Martina; Khurana, Divya S.; Cruz, Marcos; Melvin, Joseph J.; Valencia, Ignacio; Legido, Agustín; Kothare, Sanjeev V.

doi:10.1111/j.1528-1167.2007.01210.x

Cited by 44 publications

(44 citation statements)

References 27 publications

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“…It is very important to choose an appropriate AED treatment in this case because treatment with carbamazepine or oxcarbazepine may have an aggravating effect 10,19,20 in IGE. Morever, in our study, the presence of asymmetric features in JME was not associated with a poor response to a judicious anti-epileptic treatment including more recent AEDs.…”

Section: Discussionmentioning

confidence: 99%

Epileptiform Asymetries and Treatment Response in Juvenile Myoclonic Epilepsy

Létourneau

Cieuta‐Walti

Deacon

2010

Can. j. neurol. sci.

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Juvenile myoclonic epilepsy (JME) is a common idiopathic generalized and age-related epileptic syndrome. This syndrome is distinctively characterized by myoclonic jerks often associated with generalized tonic-clonic seizures (GTCS) and, less often, absence seizures 1,2 . Myoclonic seizures occur often shortly after awakening and can be precipitated by sleep deprivation and also by alcohol and photic stimulation. Usually, patients with JME respond well to appropriate treatment with valproate 3,4 . Other useful anti-epileptic drugs (AEDs) also used with other generalized epilepsies include: lamotrigine, levetiracetam and topiramate 5 .The interictal electroencephalogram (EEG) shows diffuse bilateral polyspike and slow waves (PSW) and spike and wave complexes (SWC) on a normal background 2 . The usual ABSTRACT: Background: Epileptiform electroencephalogram (EEG) asymmetries are not uncommon in juvenile myoclonic epilepsy (JME) and can contribute to the misdiagnosis of this syndrome. The objective of this study is to further characterize patients with focal or asymmetric epileptiform electroencephalographic abnormalities and more specifically in terms of response to treatment. Controversial data exists in the literature concerning this issue. Methods: We retrospectively reviewed clinical and EEG data of a group of consecutive JME patients followed at our Epilepsy Service. The first EEG available for each patient was reviewed blindly by two independent electroencephalographers. Results: Twenty-eight patients with JME were identified: 11 (39.3%) were resistant to at least one appropriate anti-epileptic drug (AED), including valproate, lamotrigine, topiramate or levetiracetam. All patients except two had generalized epileptiform abnormalities. Overall, EEG asymmetries were detected in 57.1% of the cases. The proportion of EEG asymmetries between AED-sensitive group (52.9%) and AED-resistant group (63.5%) did not reach statistical significance. Concordance between examiners for identification of EEG asymmetries was good. Analysis of patients with and without asymmetries showed no statistically significant differences in comparisons of age, family history of seizure, presence of polyspike and slow wave, photosensitivity and timing of EEG related to the onset of treatment. Conclusion: Asymmetric electroencephalographic abnormalities are frequent in patients with JME. These features should not be misinterpreted as being indicative of partial epilepsy. In our group, asymmetries were not associated with resistance to treatment.RÉSUMÉ: Asymétries épileptiformes et réponse au traitement dans l'épilepsie myoclonique juvénile. Contexte : Les asymétries épileptiformes à l'EEG sont fréquentes dans l'épilepsie myoclonique juvénile (EMJ) et peuvent contribuer à un diagnostic erroné de ce syndrome. Le but de cette étude était de mieux caractériser les patients qui ont des anomalies focales ou des anomalies asymétriques épileptiformes à l'EEG, plus particulièrement en ce qui concerne la réponse au traitement. Il existe dans la littéra...

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Section: Discussionmentioning

confidence: 99%

Epileptiform Asymetries and Treatment Response in Juvenile Myoclonic Epilepsy

Létourneau

Cieuta‐Walti

Deacon

2010

Can. j. neurol. sci.

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“…Withdrawal of OXC and introduction of the drugs used for ESES (valproate, clobazam, sulthiame, and later a cycle of steroids) led to a rapid clinical improvement. Although OXC has been demonstrated to be an effective drug for the treatment of IFEC, some papers have also shown, in the same group of epilepsies, the possibility of seizure and EEG aggravation (Chapman et al, 2003;Vendrame et al, 2007). In addition, worsening of an ongoing ESES has also been reported (Caraballo et al, 2013).…”

Section: Discussionmentioning

confidence: 99%

“…Oxcarbazepine (OXC) is a new AED that has been shown to be effective and well tolerated for the treatment of children with focal epilepsies, particularly benign epilepsy of childhood with centrotemporal spikes (BECTS) (Coppola et al, 2007). However, some reports have shown that OXC may aggravate seizures and worsen the EEG picture in children with idiopathic focal epilepsies of childhood (IFEC), including BECTS (Chapman et al, 2003;Grosso et al, 2006;Vendrame et al, 2007). Neuropsychological deterioration and exaggeration of EEG epileptic discharges during sleep, as seen in ESES, have been described following the introduction of OXC in only two children with atypical IFEC (Grosso et al, 2006).…”

Section: Introductionmentioning

confidence: 99%

Encephalopathy with status epilepticus during sleep (ESES) induced by oxcarbazepine in idiopathic focal epilepsy in childhood

Pavlidis

Rubboli

Nikanorova

et al. 2015

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SummaryEncephalopathy with status epilepticus during sleep (ESES) is an age-related disorder characterized by neuropsychological regression, epilepsy and a typical EEG pattern of continuous epileptiform activity (> 85%) during NREM sleep. Cases of worsening or induction of ESES with phenytoin, carbamazepine and phenobarbital have been reported. We describe a child with benign epilepsy with centrotemporal spikes (BECTS) in whom treatment with oxcarbazepine (OXC) induced ESES. The patient was studied through repeated clinical-neuropsychological evaluations and 24-hour EEG recordings. He was treated with OXC two months after epilepsy onset. One month after starting OXC, he developed an abrupt and severe cognitive deterioration. A 24-hour EEG and neuropsychological tests showed an electroclinical picture compatible with ESES. Withdrawal of OXC and introduction of other drugs were followed by a prompt improvement. Five months after ESES onset, a 24-hour EEG was normal. Our report indicates that OXC can induce ESES in BECTS. KEY WORDS: antiepileptic drugs (AEDs), benign epilepsy of childhood with centrotemporal spikes (BECTS), encephalopathy with status epilepticus during sleep (ESES), idiopathic focal epilepsies of childhood, oxcarbazepine (OXC).

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“…combination with other drugs or when there are other medical conditions (hyponatraemia or hyperammonaemia) (for a review: [12][13][14]). …”

Section: Box 112 Eeg and Mood Stabilisersmentioning

confidence: 99%